The exact prevalence of OCD is unknown. The National Comorbidity Survey Replication (NCS-R), a nationally representative household survey designed to assess the prevalence, severity, and comorbidity of various psychiatric disorders in the United States, found that OCD affects roughly 2.2 million American adults, or about 1% of adults in any given year [2,4]. The NCS-R researchers used criteria from the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) to make the diagnosis, based on responses to a version of the World Health Organization's Composite International Diagnostic Interview (CIDI). The Epidemiologic Catchment Area Study, conducted in the 1980s, found an OCD lifetime prevalence of 1.94% to 3.29% across five study sites [5]. This study employed lay interviewers to administer the National Institute of Mental Health Diagnostic Interview Schedule (DIS). However, the reliability of the DIS-based diagnosis is open to question; at re-interview 12 months later, only 19.2% of patients who met OCD criteria on initial interview admitted to ever having had OCD-criteria symptoms. More recent nationally representative surveys confirm that OCD has a lifetime prevalence of 2% to 3% and that it is associated with substantial comorbidity and mortality [6]. OCD is estimated to make a significant contribution to the global burden of disease, with considerable uniformity of OCD symptoms across the globe [7,8]. The incidence of OCD is reported to be higher in dermatology and cosmetic surgery patients [9].

The first step in correctly diagnosing and treating OCD is understanding its definition. Although previously considered an anxiety disorder, OCD is classified as an obsessive-compulsive disorder in the revised fifth edition of the DSM (DSM-5-TR) along with other related conditions, including body dysmorphic disorder, hoarding disorder, trichotillomania, and excoriation disorder. Essentially, OCD involves obsessions and/or compulsions that cause distress or interfere with functioning. The obsessions are usually associated with anxiety, and compulsions often serve to ameliorate that anxiety. People with the disorder are usually aware, at least at some point in time, that their obsessions or compulsions are not reasonable.

The DSM-5-TR definition of OCD is based on four criteria [22]. The first criterion is the presence of either obsessions or compulsions. Obsessions are defined by [22]:

Compulsions are defined by:

Secondly, diagnosis of OCD is dependent upon disruption of day-to-day life. The obsessions or compulsions are time consuming (take more than one hour per day) or significantly interfere with the person's normal routine, occupational (or academic) functioning, usual social activities or relationships, or other important areas of functioning.

The third diagnostic criterion is that the disturbance is not due to the direct physiologic effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition.

Disease-specific manifestations are the fourth criterion. In order for OCD to be diagnosed in patients with another Axis 1 disorder, the content of the obsessions or compulsions may not be restricted to the other disorder (e.g., preoccupation with food in the presence of an eating disorder; hair pulling in the presence of trichotillomania; concern with appearance in the presence of body dysmorphic disorder; preoccupation with having a serious illness in the presence of hypochondriasis; preoccupation with sexual urges or fantasies in the presence of a paraphilia; or guilty ruminations in the presence of major depressive disorder).

Another hypothesis regarding the underlying cause of OCD involves serotonin [36]. Research regarding a role for serotonin was spurred by studies of the effectiveness of antidepressants, such as clomipramine and desipramine, for OCD in non-depressed patients [34,39]. Clomipramine, which acts primarily as a serotonin reuptake inhibitor (SRI), has proved to be more effective than desipramine, which is thought to act primarily by inhibiting norepinephrine reuptake [40]. The ability of selective serotonin reuptake inhibitors (SSRIs) to reduce OCD symptoms further supports a role for serotonin abnormalities in the pathogenesis of OCD, a theory supported by the 2017 study in which a gene that includes a serotonin receptor, HTR2A, was found to be among the most commonly associated in those with OCD [32]. A specific mechanism, however, has not been elucidated, and studies involving measures of serotonergic function have been inconsistent.

OCPD is characterized by preoccupation with order, perfection, and control, but not by the presence of obsessions or compulsions [24]. It is often compared to a "perfectionist" personality. Unlike OCD, symptoms must appear by early adulthood for the diagnosis to be made; however, OCD and OCPD may occur in the same person. The frequency of both diagnoses occurring together is not known, but studies suggest that it is not uncommon [45]. Estimates from OCD study populations indicate a concomitant rate between 23% and 32%, although these samples were not designed to be representative of all patients with OCD [45,46]. For comparison, the prevalence of OCPD has been observed to be about 0.9% to 2% in community samples [45,46]. There is also some evidence that OCPD is more common in people with OCD than in patients with other psychiatric disorders.

Depression is a particularly common comorbidity. A chart review of 120 patients with OCD in the Netherlands found depression in one-third, and a separate structured psychiatric interview found similar results (31%) for major depression [51,52]. The Epidemiologic Catchment Area Study in the United States found 67% of individuals identified as having OCD had at least one episode of major depression [47]. In addition, OCD has been shown to comorbidly occur with social phobia (11% to 24%), simple phobia (including body dysmorphic disorder) (7% to 14%), and panic disorder (6% to 14%, 35% lifetime incidence) [9]. Associations have also been observed between OCD and other conditions, including bipolar disorder, eating disorder, generalized anxiety disorder (20%), alcohol dependence/substance abuse, and Tourette syndrome (5% to 7%) [9,10,53]. Richter and colleagues looked at patients with OCD, social anxiety disorder, or panic disorder and found that trichotillomania, skin picking, body dysmorphic disorder, and tics were more strongly associated with OCD than with the other two anxiety disorders [54].

Five SRIs are approved by the U.S. Food and Drug Administration (FDA) for OCD treatment, including four SSRIs and one serotonin-specific tricyclic antidepressant (TCA) [58]:

Clomipramine is a TCA with multiple actions, including significant activity as a serotonin reuptake inhibitor. It was the first medication approved in the United States for treatment of OCD [69]. Some studies have suggested that clomipramine is more effective than the SSRIs, but others have found equal effectiveness or more improvement with an SSRI [69,70,71,72,73]. Direct, controlled comparison studies have found fluvoxamine, paroxetine, and sertraline equal in efficacy to clomipramine. Patients with OCD who have comorbid tics or schizotypal personality are unlikely to respond to clomipramine or an SSRI alone [74]. Due to serious adverse effects, a high daily dose of clomipramine is not advised unless SSRI monotherapy is not adequate to control OCD behaviors [70]. In addition, clomipramine may be used as combination therapy with an SSRI to receive the benefits of the TCA without the problematic side effects of higher doses of the drug [70]. Concurrent use of clomipramine and fluoxetine is not advised, as fluoxetine inhibits the metabolism of clomipramine in the liver, creating high serum levels of clomipramine [70].

Although clomipramine and the SSRIs are also used to treat depression, their use in OCD has somewhat different parameters. Patients with OCD may require higher doses, and the onset of action may be slower. In depression, improvement may be expected as early as one week after initiating treatment. The APA guideline for the treatment of major depressive disorder recommends re-evaluating treatment if at least moderate improvement has not occurred after six to eight weeks [10]. In OCD, a full trial of SRI therapy takes 8 to 12 weeks, including 4 to 6 weeks on the highest tolerable dose [58,70].

Although clomipramine and the SSRIs are also used to treat depression, their use in OCD has somewhat different parameters. Patients with OCD may require higher doses, and the onset of action may be slower. In depression, improvement may be expected as early as one week after initiating treatment. The APA guideline for the treatment of major depressive disorder recommends re-evaluating treatment if at least moderate improvement has not occurred after six to eight weeks [10]. In OCD, a full trial of SRI therapy takes 8 to 12 weeks, including 4 to 6 weeks on the highest tolerable dose [58,70].

In some cases, lowering the dose, changing the timing of doses, or changing to a different SRI will help to alleviate side effects; in others, adding an additional medication may be helpful [10]. Some side effects are particularly likely with certain SSRIs. For example, paroxetine is the most anticholinergic and appears to be more likely to cause weight gain than other SSRIs. Insomnia may be addressed by taking the SSRI in the morning instead of the evening or by the addition of a sleep-promoting agent. Modafinil may help with fatigue. Excessive diaphoresis may be improved by the addition of a low-dose anticholinergic.

Sexual symptoms, including decreased libido and difficulty with orgasm, may be difficult to overcome, but there are options that will work for some patients. In some cases, sexual symptoms will decrease over time. Some patients may be willing to wait until OCD symptoms have improved and weaning from the SSRI is appropriate. Some may benefit from a "drug holiday" up to once per week, stopping the SSRI for one day before a sexual encounter. In general, stopping an SSRI abruptly is not recommended due to the possibility of withdrawal effects, but with most of the SSRIs, missing one dose is not expected to affect outcomes adversely. The short half-life of paroxetine makes it a poor choice for this technique, and the half-life of fluoxetine may be too long for the one-day "holiday" to be useful.

As noted, the APA recommends a trial of at least 8 to 12 weeks with a given SRI, including at least four to six weeks at the highest tolerable dose [10]. For patients who fail to achieve a reduction in symptoms by the end of this time or who have only minimal response, there are several APA-recommended options [10]. One strategy is to offer a trial of a different SSRI. It may take multiple trials to find the right match for a given patient. Additional options include switching to clomipramine, switching to the serotonin-norepinephrine reuptake inhibitor venlafaxine, or adding a second-generation antipsychotic. Switching to mirtazapine is also offered as a strategy, although supporting evidence is limited. Switching to venlafaxine may be less effective than switching to a different SRI.

The best duration for pharmacotherapy in OCD has not been determined. A minimum of one to two years has been recommended before withdrawal should be considered [10,90]. Others recommend that pharmacotherapy should be continued indefinitely. Data suggest that patients' symptoms will return within one to two months after medications are stopped, even after two years of successful pharmacotherapy. Up to 20% of patients who discontinue a successful drug will not respond when the drug is restarted [74]. The presence of a comorbid diagnosis can interfere with clinical recovery and may guide the choice of interventions [58]. The decision to continue or to stop medication should be individualized and discussed with each patient.

Of all potential psychological therapies for OCD, CBT is supported by the best evidence. Most studies have used some form of exposure and response prevention as the mode of therapy, with variations in frequency, intensity, and guidance. These studies have generally been small, with at most a few dozen patients. One larger, multisite trial compared exposure and response prevention to clomipramine, placebo, or a combination of the two treatments [91]. This study involved intensive, daily exposure and response prevention for four weeks, followed by maintenance sessions for another eight weeks. Overall, 71% of the 122 randomized patients completed treatment. Response rates at week 12, measured as improvement on the Y-BOCS, CGI-S, and NIMH-GOCS, were all significantly better for exposure and response prevention than for clomipramine. Exposure and response prevention plus clomipramine was not significantly better than exposure and response prevention alone. Based on the CGI-I measure, an "excellent" response was seen more often in the exposure and response prevention group and in the combination group than in the clomipramine-alone group.

Exposure and response prevention consists of a specific series of techniques. It may be offered as individual therapy or in a group setting. The APA recommends at least weekly sessions [10].

Exposure and response prevention is based on the idea that obsessions and compulsions serve to reinforce one another [97,98]. The obsessions are associated with great anxiety; because compulsions serve to reduce that anxiety, the performance of these behaviors is reinforced with each cycle. At the same time, the use of ritualized behaviors to combat anxiety prevents the development of other methods of coping with the anxious feelings. Thus, repeated exposure to a feared stimulus while avoiding the use of ritualized behavioral responses should, over time, lead to a dampening of the anxiety response and a lessening of the need to perform compulsions. Exercises generally start with exposure to a situation that causes a moderate level of anxiety and progress to exposures that are more intensely feared. Patients are encouraged to think about the feared consequences of not performing their rituals. At the same time, they are asked to abstain from these ritualistic behaviors and encouraged to develop alternative ways of tolerating and overcoming anxiety. When exposure and response prevention is successful, patients gradually become accustomed to the idea that feared outcomes are unlikely to happen even though rituals are not performed. The patient's family should be involved when possible. To be of most help to the patient, the family may need to be willing to change their responses to the patient (e.g., not provide requested reassurance to irrational doubts) [58]. Successful treatment depends in part on the family's willingness to reduce their accommodation of the patient's compulsive behaviors [99]. Additionally, a family history of OCD can significantly decrease the patient's response to CBT [100].

There is no strong evidence to support a given duration of CBT. However, the consensus, according to the APA guideline, is for an initial course of 13 to 20 weeks of weekly CBT or three weeks of daily sessions [10]. If treatment is successful, it may be tapered to monthly sessions for another three to six months. Some patients will benefit from occasional booster sessions as well. The APA recommends ongoing maintenance, although details are not specified [10]. The exact probability of relapse following CBT is unclear.

Some patients will fail to respond to both standard pharmacologic options and to outpatient CBT. Others will achieve a partial response but remain unable to return to a satisfactory level of functioning. A subset of patients will be so disabled by symptoms that they are unable to participate in standard outpatient treatment. These patients should generally be referred to specialty psychiatric care, preferably to a physician with expertise in OCD.